Oncogenic cases of EBV, involving a chromosome shift are associated with the impairment of cell mediated immunity.  They are seen most often in conjunction with:
1.  congenital immunodeficiency, such as X-linked immunodeficiency syndrome
2.  organ transplant cases involving immunosuppressive drugs
3.  HIV patients, usually, but not always, when the CD4 count is indicative of AIDS. (3)

X-linked Lymphoproliferative Disease
EBV-positive lymphoma is associated with this genetic immunodeficiency disorder.  The patient's T-cells are unable to appropriately regulate B-cells which are unable to produce antibodies against EBV antigens such as  EBNA (EBV nuclear antigens).  Post EBV infection, over 60% develop fatal infectious mononucleosis and 20% develop an EBV-positive lymphoma (4).

Post-Transplant Lymphoproliferative Disease (PTLD)
For similar reasons as above, organ or bone marrow transplant recipients are at risk for developing B-cell lymphomas.  Induced immunosuppression, necessary for the transplant to be accepted, leads to a loss of control over EBV infection.  Serologically, there is enhanced production of antibodies against the viral capsid antigen (VCA) and early antigens (EA) but a failure to respond to EBNA.  The lymphomas which develop contain parts of the latent EBV genome, expressing individual EBNAs and latent membrane protein 1 (LMP-1).  EBNA2 and LMP-1 are targeted by the CTL response in healthy individuals.  For this reason, the tumors usually regress with restored immune function (4).

EBV and AIDS
The most frequently observed opportunistic malignancy accompanying HIV-1 infection is non-Hodgkin's lymphoma.  These lymphomas are grouped into several categories: small non-cleaved-cell lymphoma (SNCCL), diffuse large cell lymphoma (DLCL), anaplastic large-cell lymphoma (ALCL), and body-cavity based lymphoma (BCBL) (6).  In patients using antiretroviral therapy, 29% developed NHL lymphomas after three years of treatment (4).  About half of these NHL tumors are EBV positive.  This includes primary CNS lymphomas, 35-40% of Burkitt's lymphomas, and 50-60% of non-Burkitt's lymphomas (4).  The prevalence of EBV in oral lesions and oral neoplasms of HIV patients has been confirmed by PCR and Southern blot analysis.  Using these same methods, EBV has also been detected in hairy leukoplakia lesions, in a subset of AIDS related lymphomas, and in saliva from HIV-positive persons (5).  AIDS-SNCCL is infected by EBV in 30% of cases, AIDS-DLCL is characterized by EBV in the majority of cases, and AIDS-BCBL is associated with EBV in almost all cases (6).
 
 

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References for Epidemiology pages

1. Niederman, J.C., Evans, A.S.  "Epstein-Barr Virus."  Viral Infections of Humans: Epidemiology and Control.  New York: Plenum, 1997; 253-283.
2. Henle, G., Henle, W.  Observations on childhood infections with the Epstein-Barr virus.  J. Infect. Dis.  1970; 123: 303-309.
3. Evans, A.S., Mueller, N.E.  "Epstein-Barr Virus and Malignant Lymphomas." Viral Infections of Humans: Epidemiology and Control.  New York: Plenum, 1997; 895-933.
4. de-Thé, G. "Nasopharyngeal Carcinoma." Viral Infections of Humans: Epidemiology and Control.  New York: Plenum, 1997; 935-967.
5. Webster-Cyriaque, J., Edwards, R.H., Quinlivan, E.B., Patton, L., Wohl, D., Raab-Traub, N. Epstein-Barr virus and human herpesvirus 8 prevalence in human immunodeficiency virus-associated oral mucosal lesions. J. Infect. Dis. 1997; 175: 1324-1332.
6. Gaidano, G., Pastore, C., Gloghini, A., Volpe, G., Ghia, P., Saglio, G., Carbone, A.  AIDS-related non-Hodgkin's lymphomas: molecular genetics, viral infection and cytokine deregulation.  Acta Haematol. 1996; 95(3-4): 193-198.